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Cough reflex suppression" refers to the inhibition or dampening of the neural reflex arc responsible for producing cough. The cough reflex is primarily mediated by sensory vagal afferent fibers (including Aδ and C fibers) in the airways, which detect mechanical, chemical, and inflammatory stimuli and signal via the vagus nerve to the brainstem, culminating in the motor response of coughing. Pharmacological suppression of the cough reflex is achieved by targeting specific neural pathways in the periphery (e.g., P2X3 receptors responsive to ATP, TRPV1, TRPA1) or centrally (e.g., mu opioid, NMDA, GABA_B, sigma, sodium channels). Several drugs act through these mechanisms, but "cough reflex suppression" itself is not a single molecular target—it is the outcome of modulating these underlying pathways.
Inhibition of central or peripheral neural transmission in cough pathways (e.g., via mu opioid, NMDA, GABA_B, or P2X3 receptors); Blockade of purinergic signaling at airway afferents (e.g., P2X3 antagonism); Central suppression of medullary cough center activity
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